1. Anosmia refers to complete loss of sense of smell (olfaction); hyposmia refers to
reduction in sense of smell. Either may be temporary or permanent. Other olfactory
disturbances include distortions of normal smells (parosmia or dysosmia) and a heightened
sense of smell to some or all odourants (hyperosmia).
2. Taste and smell rely on chemical substances to stimulate their receptors and together form
the chemosensory system. Their combination produces the sensation of flavour and
dysfunction in one is often perceived as abnormality in the other.
3. There are two well-characterised nasal chemosensory systems: the free nerve endings of
the trigeminal nerve and the sensory receptors of the olfactory nerve. A third, vomeronasal,
organ exists but is of doubtful function in humans.
4. The free trigeminal nerve endings in the walls of the nasal passages respond non-
selectively to a wide variety of volatile chemical substances, including high concentrations
of most odourants. The olfactory receptors respond to chemical stimuli at lower
concentrations and with far greater selectivity than trigeminal endings. In total anosmia,
the capacity to distinguish between odours is lost, but the response to nasal irritation is
5. Olfactory function can be disrupted in three ways, the second and third of which are
5.1. By nasal obstruction preventing volatile substances from reaching the receptors -
5.2. By impairment of receptor or cranial nerve function - sensory olfactory loss.
5.3. By pathological processes affecting pathways from the olfactory bulb (the termination
of the first cranial nerve) to the olfactory cortex and other parts of the brain.
6. Olfactory impairment is not always permanent. The receptor neurones have a lifespan
limited to about 30 days, with continual replacement. This is an important factor in
recovery from anosmia of certain causes, which may take months. Recovery of olfaction
occurs in 2/3 of cases with cranial nerve palsy, sometimes as long as five years later.
7. Qualitative changes in smell may be complained of in association with quantitative
impairment and both may be accompanied by a perceived disturbance of taste.
They rely on measuring minimal perceptible odour, identification, or adaptation. Even
objective tests, using physiological measurements or evoked responses, may or may not
be positive. In clinical practice, simple tests of identification of and discrimination between
familiar substances. Appreciation of an odour, despite the inability to name it, excludes
may indicate a focal neurological lesion.
10. Cases of malingering can sometimes be exposed by comparing responses to odourants
which differ in their propensity to stimulate trigeminal nerve endings. These are invariably
stimulated by, for example, ammonia.
11. Causes of anosmia and hyposmia can be classified thus:
11.1. Lesions of the Nose
11.1.1. Deviated nasal septum is a rare cause of disturbance of smell. Simple
anatomical defects do not usually result in an abnormality of smell.
11.1.2. Nasal polyps
11.1.3. Allergic and vasomotor rhinitis are common causes of abnormalities of
smell, but only rarely is the associated loss of smell total. In conditions such
as hay fever and the common cold, the loss of smell is temporary.
11.1.4. Infective rhinitis may damage considerable areas of olfactory mucosa if it
becomes chronic and the affected areas do not regenerate.
11.1.5. Tumours, including papilloma, adenoma, squamous cell carcinoma,
esthesioneuroepithelioma and idiopathic midline granuloma.
11.1.6. Toxic fumes may cause loss of smell, as may heavy smoking.
11.2. Lesions of the olfactory nerves.
11.2.1. Injury, either through a direct blow or from an occipital blow with shearing of
nerve fibres, usually causes immediate and complete loss of smell.
11.2.2. Viral infections such as influenza can cause great damage to the olfactory
nerve fibres, replacing all the neuronal tissue with fibrous tissue.
11.2.3. Meningitis, sarcoid and neurosyphilis may damage the olfactory tract.
disease, motor neurone disease and multiple sclerosis (olfactory
dysfunction occurs in about 40% of patients with MS)
11.3. Intracranial Lesions.
11.3.1. Trauma tends to give complete loss.
11.3.2. Intracranial tumours can affect the sense of smell in two ways, either by
pressure on the olfactory nerve fibres or bulb, or by interference with the
intracerebral pathways. Osteomas or meningiomas of the anterior fossa
tend to diminish the sense of smell and at first this is unilateral. Frontal lobe
tumours may do the same.
11.3.3. Obstructive hydrocephalus.
11.4. Systemic diseases in which the sense of smell may be impaired include diabetes
mellitus, Paget's disease of bone, polyarteritis, cystic fibrosis and cirrhosis.
11.5. Iatrogenic causes include rhinoplasty, intracranial surgery, radiation therapy and
11.6. Psychogenic Disorders.
Psychiatric disorders such as psychoses (including Korsakoff's), depression and
and there is a specific olfactory reference syndrome. Hysteria and malingering
have a place amongst these disorders. Olfactory hallucinations may also occur in
Alzheimer's disease and alcohol withdrawal.
11.7. Anosmia is occasionally congenital, sometimes hereditary.
12. Anosmia and hyposmia are disturbances of the sense of smell which may be temporary
or permanent. There are many possible causes, most of which are listed above. Many
cases of anosmia and hyposmia resolve naturally, so no treatment is necessary. In others,
treatment is that of the underlying cause, but the impairment is permanent in some cases.
Finelli P.F. & Mair R.G. Disturbances of Taste and smell, in (eds) Bradley et al, Neurology in
Clinical Practice, 3
Ed. 2000, Boston Butterworth Heinemann, p.263-7.
Otolaryngology. Volume 4. Rhinology. 6
Ed. 1997. Oxford. Butterworth-Heinemann. p. 4/5/1-
Ed. 2001. Oxford.
Leopold D. Disorders of olfactory perception: diagnosis and treatment. In Chem. Senses 2002